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Show IOl/mal of Cli..ical Neur(l-ophlhalmology 7(4): 223-226, 1987. Cavernous Sinus Infection Manifested by Horner's Syndrome and Ipsilateral Sixth Nerve Palsy Benjamin Hartmann, M,D" Israel Kremer, M,D., Isaac Gutman, M.D., David Krakowski, M.D., and Jacob Kam, M.D. ~, 1987 Raven Press, Ltd., New York A 20-year-old man presented with a left sixth nerve paresis associated with ipsilateral Horner's syndrome several days after surgical drainage of a facial abscess. This unusual association between sixth nerve palsy and Horner's syndrome is presented and its neuroanatomic correlation is discussed. Key Words: Horner's syndrome-Abducens paresisIntracavernous sympathetic branch-Cavernous sinus thrombosis-Cavernous sinus infection. From the Department of Ophthalmology (B. H., IX, O.K., ].K.), Assaf-Harofeh Medical Center, Zeriffin, and the Neuroophthalmology Unit (I.G.), Chaim Sheba Medical Center, TelHashomer, Israel. Address correspondence and reprint request to Benjamin Hartmann, M.D., Department of Ophthalmology, Assaf Harofeh Medical Center, Zeriffin, 70300, Israel. 223 Isolated sixth nerve palsy associated with ipsilateral Horner's syndrome is a rare clinical entity. It was Parkinson (1-3) who confirmed Monro's observation (4) of a large sympathetic nerve joining the sixth cranial nerve in the cavernous sinus. Abad et al. (5) have subsequently described parasellar carotid aneurysm as an etiologic cause. Others have described this rare association in cases of intracavernous meningiomas (6,7). Cavernous sinus infection and thrombosis is presently an uncommon disease because of the frequent use of antibiotics. We have found no report in the English literature on the association of cavernous sinus infection with the above described rare neurologic syndrome, and, therefore, we present a case of a young patient with isolated sixth nerve paresis associated with Horner's syndrome caused by this infection. CASE REPORT A 21-year-old white man noticed a furuncle on his left upper cheek on October 19, 1985. Four days later the furuncle developed into an abscess, and his fever rose to 40°C. The abscess was drained, and a combination of oral cloxacillin, 500 mg q6h, and amoxicillin, 500 mg q8h, was started. The next day his temperature spiked to 40.6°C, and as he was found to be lethargic and complaining of severe headaches, we decided to admit him. His general physical and ophthalmological examinations were unremarkable, and no signs of meningeal irritation were found. The pupils were round and equal, and no ptosis was noticed. The laboratory workup revealed leukocytosis of 224 B. HARTMANN ET AL. 23,400, and X-ray examination of the paranasal sinuses revealed no abnormality. Three days later (October 28), his general condition started to improve, the temperature decreased to 37.6°C, and a left periorbital cellulitis was noted. Repeated blood cultures were positive for coagulase-positive Staphylococcus aureus, and therefore intravenous cloxacillin and gentamicin in combination with oral erythromycin were initiated. On October 30 his condition improved significantly, he was afebrile, and the signs of periorbital cellulitis resolved completely. At that time, the patient started to complain of diplopia on left gaze. The neuroophthalmological examination showed a visual acuity of 6/6 with myopic correction in both eyes and normal color vision. The anterior segments, intraocular pressure, and fundus were normal. A mild ptosis of 2 mm in the left eye was noticed (Fig. 1), and examination of the ocular movements showed a slow abducting saccade of the left eye. The alternate cover test showed one diopter of esotropia on right gaze that increased to 16 diopters of esotropia on left gaze and to 6 diopters in primary position. Diplopia test, done with red green goggles, disclosed uncrossed diplopia, maximal on left gaze. This finding was also confirmed by a Hess screen test. The pupils measured 5 mm in the right and 3 mm in the left, (Fig. 1). Ten percent cocaine drops dilated the right pupil only (Fig. 2). Diagnosis of left sixth nerve paresis with ipsilateral Horner's syndrome was made. A high resolution, computed tomography (CT) scan directed to the area of the cavernous sinus (Fig. 3) showed diffuse opacification of the left cavernous sinus that supported the diagnosis of cavernous sinus infection. Subsequently the patient was treated with heparin i.v. in addition to antibiotic therapy, and, owing to the possibility of secondary cavernous sinus thrombosis, this treatment was continued for 3 more weeks. Repeated neuro-ophthalmological follow-up examinations showed no change in the patient's left ptosis, miosis, and sixth nerve paresis, even 12 months later. DISCUSSION According to Parkinson's anatomic findings, (1-3) the sympathetic nerve is a single trunk that runs with the carotid artery. In the vicinity of the cavernous sinus it joins the abducens nerve briefly before joining the ophthalmic branch of the trigeminal nerve (1,6). Although Parkinson never encountered this association clinically, he predick':! th,o I)(i""ihility of .1 syndrome that might re- FIG. 1. Left ptosis, left miosis. suit from an intracavernous lesion along the short segment of the sixth cranial nerve accompanied by the sympathetic nerve. In 1981, Abad et al. (5) published a description of an unrecognized neurological syndrome: a sixth nerve palsy associated with Horner's syndrome due to traumatic intracavernous carotid aneurysm. Gelber and Sundt (8) reported 10 cases of intracavernous giant aneurysm, while one of those patients had an intrapetrous- intracavernous aneurysm presenting clinically as an isolated sixth nerve palsy associated with Horner's syndrome. Miller (6) has seen this syndrome in a patient with an intracavernous meningioma and in another with a nasopharyngeal carcinoma. None of the latter two patients had any other neurologic symptoms and signs. Thompson and Mensher (9) have described a sixth nerve palsy associated with Horner's syndrome and corneal hypoesthesia in patient no.n of their series. The cause was an infraclinoid carotid aneurysm. Gutman et. al. (7) have recently described isolated sixth nerve palsy associated with Horner's syndrome in one patient with intracavernous carotid aneurysm and a second with an intracavernous meningioma. Cavernous sinus thrombosis was encountered much more frequently in the preantibiotic era (10). It usually complicates purulent infection of the face, mouth (11), and nasal cavities as a complication of maxil- FIG. 2. Positive cocaine test showing dilatation of the right pupil only. CAVERNOUS SINUS INFECTION AND HORNER'S SYNDROME 225 FIG. 3 (A) Axial CT with double contrast showing hyperdense lesion in the left cavernous sinus. (B) Coronal cut, showing the same lesion. lary surgery (12), extraction of teeth (13), infection of the throat and middle ear, and sphenoid sinuses. In the majority of cases, the cavernous sinus was infected via the bloodstream. The bacteria most commonly involved in this serious condition were Streptococcus, Staphylococcus aureus, Meningococcus, Pneumococcus, and Pyocyaneus (10). The full clinical picture includes headaches, spiky fever, chills, sweating, and tachycardia. The ocular signs consist of conjunctival edema, ptosis, lid swelling, chemosis, exophthalmos, and ophthalmoplegia, which is caused by involvement of the third, fourth, and sixth cranial nerves in the cav-ernous sinus. Rarely, cavernous sinus thrombosis may cause blindness (14,15). Cavernous sinus thrombosis is now rarely seen because of the common use of potent systemic antibiotics. This treatment may modify the clinical picture of this lethal disease, whose neuro-ophthalmological signs may include only sixth nerve paresis and Horner's syndrome, as happened in our young male. In this patient, the etiologic cause was a combination of partial cavernous sinus thrombosis and infection complicating a facial skin abscess. The evidence for this pathogenetic mechanism was found by computed axial tomography done with a double amount of contrast material. Early recognition of this rare clinical association prompted immediate intensive antibiotic treatment that probably prevented further evolution of the full clinical picture of cavernous sinus thrombosis (10-14). Awareness of this rare clinical syndrome and the use of a proper technique of CT scanning directed to the parasellar area with thin cuts of axial and coronal views may help the clinician to prevent deterioration of this potentially lethal disease (16-18). REFERENCES 1 Parkinson D, johnston j, Chaudhari A. Sympathetic connections of the fifth and sixth cranial nerves. A,UII Rec 1978;191:221-6. 2. Parkinson D. Bernard, Mitchell, Horner svndromes and others7 Surg Neu/'[ll 1979; 11 :221-3. - 3. johnston M, Parkinson D. Intracranial svmpathetic pathways associated with six cranial nerve. I Neurosurg 1974;39:236-·n 4. Monro A. The allaloml/ of Ihe humall DOlles alld Ilcrpes. Edinburgh: Hamilton and' Balfour, 1746;363. 5. Abad j, Alvarez F. Blazquez M. An unrecognized neurological syndrome: sixth nerve palsy and Horner's syndrome due to traumatic intracavernous carotid aneurysm. Surg NeuroI1981;lb:140-4. - 6. Miller RN. Walsh alld Hoyt's dl1licallleuro-ophlhalmologll. 4th ed. Baltimore Williams and Wilkins, 1985;425-8, 703-5, 1012-5. 7. Gutman I, Levartovski S, Goldhammer Y, Tadmor R, Findler G. Sixth nerve palsy and unilateral Horner's syndrome. Ophthalmologlf 1986;93:913-6. 8. Gelber B, Sundt T. Treatment of intracavernous and giant carotid aneurysm by combined internal carotid ligation and extra to intracranial bypass. I Neu/'[lsurg 1980;52:1-10 9. Thompson S, Mensher j. Adrenergic mydriasis in Horner's syndrome: The hydroxyamphetamine test for diagnosis of postganglionic defects. Am IOplllhalmoI1971;72:472-80. 10. Walsh F, Hoyt W. Clillical Ilfuro-ophllwlmology, 3rd ed. Baltimore: Williams and Wilkins, 1969;1892-4. 11 Harbour R, Trobe j, Ballinger W. Septic cavernous sinus thrombosis associated with gingivitis and parapharyngeal abscess. Arch 01'hlhalmoI1984;102:94-7. 12. Stern N, Shensa D, Trop R. Cavernous sinus thrombosis: a complication of maxillary surgery. I Oral Surg 1981;39: 436-9. JClill Ncura-ol"lthalmol, Vol. 7, Na. 4, 1987 226 B. HARTMANN ET AL. 13. Stevens J, Robinson K. Chronic cavernous sinus thrombosis: discussion and report of case. f Oral Stag 1977;35: 136-9. 14. Friberg T, Sogg R. Ischemic optic neuropathy in cavernous sinus thrombosis. Arch Ophthalmol 1978;96:453-6. IS. Geggel H, Isenberg S. Cavernous sinus thrombosis as a cause of unilateral blindness. A/l/l OphthalmoI1982;14:56974. I ,-li/l .',r.ili,.' 16. Peyster R, Hoover E. Computerized tomography in orbital disease a/ld /leuro-ophthalmology, 1st ed. Chicago: Yearbook medical Publishers, 1984;153-67, 263-87. 17. Kline L, Chandra-Sekar B. Pitfalls in computed tomographic evaluation of the cavernous sinus. Surv Ophthalmol 1985;29:293-6. 18. Kline L, Acker J, Post J. Computed tomographic evaluation of the cavernous sinus. Ophthalmology 1982;89:374-85. [CLcavernoussinusthrombosis] |
